Diminished glucose availability (glucoprivation) causes increased food intake in most mammals. Since glucoprivation is a physiological emergency and does not normally occur in association with spontaneous feeding, some investigators have suggested that the glucoprivic control of feeding behavior is not relevant to the day-to-day management of ingestion. However we have demonstrated that feeding initiated by glucoprivation continues to occur after glucose availability is restored. Furthermore the spontaneous termination of glucoprivic feeding does not seem associated with signs of glucorestoration. These findings have raised the possibility that this control may affect feeding under circumstances other than during acute glucoprivic crisis. The experiments proposed here will, 1) Further investigate the conditions under which glucoprivic feeding behavior can be maintained in the absence of apparent glucoprivation, 2) Determine the relationship between the biochemical effects of glucoprivation, gastrointestinal factors, and the initiation and termination of glucoprivic feeding behavior, 3) Utilize some newly developed techniques to assess the role of brain glucoreceptors and brain catecholamine neurons in the glucoprivic control of feeding.